Evidence map›Paper›PMID 40422220›Full record

ReviewCells2025

The Metabolic Landscape of Cancer Stem Cells: Insights and Implications for Therapy.

Martina Milella, Monica Rutigliano, Savio Domenico Pandolfo, Achille Aveta, Felice Crocetto, Matteo Ferro, Antonio d'Amati, Pasquale Ditonno, Giuseppe Lucarelli, Francesco Lasorsa

Abstract readReview
In one paragraph

Review in Cells, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

30 citing papers in PubMed.

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  14. Metabolic reprogramming and plasticity of cancer stem cells.Frontiers in cell and developmental biology · 2026
    Review
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  17. The authors respond to feedback onFrontiers in oncology · 2026
    Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors.

Martina MilellaUrology and Kidney Transplantation Unit, Department of Precision and Regenerative Medicine and Ionian Area-Urology, University of Bari "Aldo Moro", 70124 Bari, Italy.
Monica RutiglianoUrology and Kidney Transplantation Unit, Department of Precision and Regenerative Medicine and Ionian Area-Urology, University of Bari "Aldo Moro", 70124 Bari, Italy.
Savio Domenico PandolfoDepartment of Urology, University of L'Aquila, 67100 L'Aquila, Italy.ORCID 0000-0001-9621-3059
Achille AvetaDepartment of Urology, University of L'Aquila, 67100 L'Aquila, Italy.ORCID 0000-0001-8470-1995
Felice CrocettoDepartment of Urology, University of L'Aquila, 67100 L'Aquila, Italy.ORCID 0000-0002-4315-7660
Matteo FerroUrology Unit, Department of Health Science, University of Milan, 20122 Milan, Italy.
Antonio d'AmatiUrology and Kidney Transplantation Unit, Department of Precision and Regenerative Medicine and Ionian Area-Urology, University of Bari "Aldo Moro", 70124 Bari, Italy.ORCID 0000-0002-4810-1201
Pasquale DitonnoUrology and Kidney Transplantation Unit, Department of Precision and Regenerative Medicine and Ionian Area-Urology, University of Bari "Aldo Moro", 70124 Bari, Italy.ORCID 0000-0001-7718-7676
Giuseppe LucarelliUrology and Kidney Transplantation Unit, Department of Precision and Regenerative Medicine and Ionian Area-Urology, University of Bari "Aldo Moro", 70124 Bari, Italy.ORCID 0000-0001-7807-1229
Francesco LasorsaUrology and Kidney Transplantation Unit, Department of Precision and Regenerative Medicine and Ionian Area-Urology, University of Bari "Aldo Moro", 70124 Bari, Italy.ORCID 0000-0001-8884-0757

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cancer stem cells (CSCs) are a subpopulation with self-renewal and differentiation capacities believed to be responsible for tumor initiation, progression, and recurrence. These cells exhibit unique metabolic features that contribute to their stemness and survival in hostile tumor microenvironments. Like non-stem cancer cells, CSCs primarily rely on glycolysis for ATP production, akin to the Warburg effect. However, CSCs also show increased dependence on alternative metabolic pathways, such as oxidative phosphorylation (OXPHOS) and fatty acid metabolism, which provide necessary energy and building blocks for self-renewal and therapy resistance. The metabolic plasticity of CSCs enables them to adapt to fluctuating nutrient availability and hypoxic conditions within the tumor. Recent studies highlight the importance of these metabolic shifts in maintaining the CSC phenotype and promoting cancer progression. The CSC model suggests that a small, metabolically adaptable subpopulation drives tumor growth and therapy resistance. CSCs can switch between glycolysis and mitochondrial metabolism, enhancing their survival under stress and dormant states. Targeting CSC metabolism offers a promising therapeutic strategy; however, their adaptability complicates eradication. A multi-targeted approach addressing various metabolic pathways is essential for effective CSC elimination, underscoring the need for further research into specific CSC markers and mechanisms that distinguish their metabolism from normal stem cells for successful therapeutic intervention.

Indexed as

NeoplasmsNeoplastic Stem CellsAnimalsGlycolysisHumansMitochondriaOxidative PhosphorylationTumor Microenvironmentcancermarkersstem cellstreatment

Identifiers

PMID40422220
PMCPMC12109792

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.